[Men and alcohol; historical view].
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Biomedical subjects
Publications and source records attributed to T Takasu.
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Virus-related neurological diseases (VRNDS) are classified according to, (1) the site of main pathologic changes, (2) the type of cells infected with (parasitized by) pathogenic viruses, (3) the species of causative viruses. In the acutenesis of the development of clinical manifections and (5) the length of latency (period between infection and the onset of the illness). VRNDs were classified into meningitides, encephalitides, myelitides and neuritides. The VRNDs in which nerve cells (neurons, neuroglial cells or both) are parasitized by pathogenic viruses can be called neuroinfective viral neurological diseases. The VRDs in which nerve cells can be called non neuro-infective neurological viral disease. VRNDs were classified into those by Papova viruses, those by Herpes viruses, those by Picornaviruses, those by Toga viruses, those by Flaviviruses, those by Paramyxoviruses, those by Rhabdoviruses, those by Arenaviruses, those by Buniaviruses and those by Retroviruses. VRNDs may develop acutely, subacutely on chronically. There are VRNDs that can be called progressive because their course is progressive and their outcome is fatal. Some VRNDs develop soon after primary infection and other VRNDs develop long after primary infection on reactivation of the virus.
To evaluate the annual incidence of viral CNS infections in Japan, a questionnaire was delivered to the related departments of hospitals and an answer was given from 377 departments (30.2%). Etiological analysis of patients with viral meningoencephalitis indicates that the most (64%) among those with encephalitis diagnosed, is herpes simplex virus (HSV) encephalitis, and the most (89%) among those with viral meningitis diagnosed is non-polio enterovirus (EV) meningitis, followed by mumps virus (MV) meningitis (9%). Epidemiological findings of CNS infections with three viruses, HSV, EV, and MV, are different from each another in age distribution or in seasonal and epidemic incidence, similar to European and American findings, except that with Japanese encephalitis virus (JEV). Infections with JEV decrease recently to 2-39 cases/year by control measures for many years in Japan, though the infections with JEV continue to occur in continental Asian countries. In addition to JE, Japanese travellers abroad should be treated to be protected from infectious diseases absent in Japan, such as rabies.
Clinical data indicate that the recurring herpes simplex virus (HSV) from oro-labial lesions is HSV subtype 1 and that the virus from genital lesions is HSV-2. This suggests that HSV-1 and HSV-2 reside in latent forms in the trigeminal ganglia and sacral ganglia, respectively. However, the distribution of latent HSV-1 and HSV-2 infections in human spinal ganglia has not been fully examined. This report concerns the application of polymerase chain reaction (PCR) and in situ hybridization (ISH) to such a study. By using PCR and employing the respective primers, HSV-1 and HSV-2 DNAs were detected in 207 of 524 samples from 262 spinal ganglia (from the cervical to the sacral ganglia) examined on both sides. The percentages of HSV-1 and HSV-2 detected in a given set of ganglia were similar, indicating an absence of site preference. By ISH, few but positive hybridization signals were detected evenly in sacral ganglia sections. The data suggest that regional specificity of recurrent HSV infections is not due to regional distribution of latent virus, but that local host factors may be important for recurrences.
Varicella-zoster virus (VZV) reactivation without cutaneous vesicles (zoster sine herpete) has been demonstrated in 8 to 25% of patients with acute peripheral facial palsy (APFP) by serological methods. To make an early diagnosis of zoster sine herpete, VZV DNA in oropharyngeal swabs from patients with APFP was examined by the polymerase chain reaction (PCR). VZV DNA was detected in oropharyngeal swabs from 6 of 36 (17%) patients with APFP by PCR. VZV DNA was detected in the oropharyngeal swabs from the six patients at their initial visit (2 to 4 days after the onset of APFP), while the anti-VZV IgM and IgG antibody titers were not increased significantly. In contrast, VZV DNA was undetectable in the oropharyngeal swabs at the time when the VZV specific antibody response appeared. These results indicate that detection of VZV DNA in oropharyngeal swabs by PCR is more useful than currently available serological assays for the early diagnosis of zoster sine herpete in patients with APFP.
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Bilateral striatal necrosis in acute encephalopathy has been reported in a small number of adults with methanol or cyanide intoxication, hypoxic encephalopathy or haemolytic-uraemic syndrome. Acute encephalopathy with bilateral striatal necrosis has been reported in infants and children. However, the pathogenesis of the necrosis remains unclear. This is the first report of serial imaging from the very early to chronic stage in two acute encephalopathic adults with bilateral striatal necrosis. A clinicoradiological study is presented for clarification of the pathological process and pathogenesis. Striatal lesions were not detected in the very early stages, but only thereafter. Serial studies suggested that the lesions were caused by delayed neuronal death. These patients had severe lactic acidosis, near the limit for survival. There have been few reports of adults with acute encephalopathy and bilateral striatal necrosis in whom arterial pH was described; all these exhibited marked acidosis. The common pathophysiological condition among these encephalopathies with bilateral striatal necrosis could be lactic acidosis elicited by impairment of ATP generation through the Krebs cycle. The striatum might represent one of the target areas of Krebs-cycle blockade.
We present the unusual case of 16-year-old girl who developed intractable convulsions five days after the onset of a cold. Meningeal signs, lymphopenia, proteinuria, and lupus anticoagulant were also present. Treatment with anticonvulsants, antituberculous agents, and adenine arabinoside were ineffective. The initiation of methylprednisolone pulse therapy immediately resolved convulsions and fever. The diagnosis, suggested by the clinical course and the marked improvement of the meningoencephalitis by pulse therapy, was an encephalitic form of acute disseminated encephalomyelitis. Clinical and laboratory findings indicated that an immune disorder may have triggered an abnormal response to a viral infection leading to this patient's neurologic disorder.
Annexin I is a calcium- and phospholipid-binding protein that is involved in the regulation of cellular differentiation. The aim of the present study was to determine the localization of annexin I mRNA expression in normal and diseased human skin. In situ hybridization with a specific digoxigenin-labelled RNA probe was used throughout. We detected no annexin I mRNA signals in basal and suprabasal cells of normal epidermis, but positive signals were evident in the sudoriferous ducts. Annexin I mRNA expression was detected in the keratinizing squamous cells in keratotic type seborrhoeic keratosis and in keratinocytes at the periphery of the horn pearl in well-differentiated squamous cell carcinoma. Positive signals were also seen at the border between involved and noninvolved skin in psoriasis vulgaris and in dyskeratotic epidermal keratinocytes in keratosis follicularis Darier. By contrast, no annexin I mRNA signals were detected in tumour cells in basal cell carcinoma. The present results suggest that annexin I expression is related to, and may play a role in, keratinization disorders.
Central motor conduction time and regional cerebral blood flow were measured before and 20 min after intravenous injection of 17 mg/kg acetazolamide in 10 patients with periventricular lucencies (PVL) and 10 age-matched healthy controls. Central motor conduction time was measured using a magnetic stimulator and regional cerebral blood flow was measured by stable xenon computed tomography method. The central motor conduction time was significantly longer in the patients with PVL than in the healthy controls and was shortened significantly by the intravenous injection of acetazolamide in the patients with PVL. The blood flow not only in the periventricular white matter but also in the cerebral cortex and the cerebral white matter was significantly lower in the patients with PVL than in the healthy controls. The intravenous injection of acetazolamide increased significantly the regional cerebral blood flow except in the PVL areas. The prolongation of the central motor conduction time may be at least partly related with decreased blood flow in the cerebral cortex and cerebral white matter.
This is the first report on the evaluation of treatment with fasudil hydrochloride, a novel intracellular calcium antagonist, for wandering symptoms in patients with cerebrovascular dementia by using 31P-magnetic resonance spectroscopy (MRS) and Xe-computed tomography (CT). The subjects studied were two patients with cerebrovascular dementia who had had frequent wandering episodes. The clinical diagnosis was Binswanger-type cerebral infarction in patient 1 and sequelae of cerebral bleeding and multiple lacunar infarctions in patient 2. Treatment with fasudil at 30 or 60 mg/day was given orally for 8 weeks. The wandering symptoms disappeared in both patients during the treatment and reappeared a few days after discontinuation of the treatment. Mental tests indicated that memory was mildly improved during the treatment. Pretreatment 31P-MRS findings revealed decreases in relative signal intensities of phosphomonoester and phosphodiesters and an increase in that of mean adenosine triphosphates. After treatment, these findings disappeared. The regional cerebral blood flow values by Xe-CT in both patients did not show significant changes from before treatment to the values after treatment. These results suggest that the efficacy of fasudil for the wandering symptoms and mental function observed in our patients may have been related to a direct effect on intracellular energy metabolism.
The present study was designed to examine the effects of sodium ozagrel on hemostatic markers and cerebral blood flow in lacunar infarction. Ten cases of lacunar infarction in which sodium ozagrel was given (administered group), 10 cases of lacunar infarction in which sodium ozagrel was not given (nonadministered group), and 10 age-matched controls in which cerebrovascular diseases were absent but risk factors were similar to those of the patients (control group) were studied. Intravenous infusion of 80 mg of sodium ozagrel was done twice a day for 2 weeks. Platelet factor 4, beta-thromboglobulin, and fibrinopeptide A were significantly higher in the administered and nonadministered groups than in the control group at the time of admission. Platelet factor 4, beta-thromboglobulin, fibrinopeptide A, and thromboxane B2 were decreased significantly by the administration of sodium ozagrel. The blood flow in the cerebral cortex was significantly lower in the administered and nonadministered groups than in the control group. The blood flows around the infarcted area, in the cerebral cortex, and in the cerebral white matter were significantly increased by the administration of sodium ozagrel. Sodium ozagrel is considered to decrease platelet aggregation and increase cerebral blood flow by decreasing thromboxane A2, which has a platelet-aggregating and a vasoconstricting action. Sodium ozagrel is considered to be effective in the acute phase of lacunar infarction.
The aims of this study were to investigate the effect of aminoguanidine (AG) on slowing of motor nerve conduction velocity (MNCV) of the sciatic nerve in streptozocin-induced diabetic rats and to assess its mechanism of action. The MNCV of the sciatic nerve was measured electrophysiologically in diabetic rats treated with and without AG for 16 weeks. To elucidate the action of AG, morphological lesion and abnormality of polyol pathway metabolism in the nerve were examined and tissue levels of advanced glycosylation end-products (AGE) were determined as an indicator of AGE accumulation in tissue. Diabetic rats were treated with AG at three doses of 10, 25 and 50 mg/kg for 16 weeks. Myelinated fiber morphometry and nerve Na+,K(-)-ATPase activity were determined. The AGE levels in renal cortex were measured by a specific ELISA. Aminoguanidine dose-dependently ameliorated slowing of MNCV 16 weeks after the treatment without changing body weight or blood glucose levels. No difference in myelinated fiber morphometry or Na+,K(+)-ATPase activity with or without AG treatment was detected in diabetic rats. Diabetes increased the AGE level in the renal cortex by six times compared to non-diabetic rats, and AG reduced the rise in the AGE level by 40%. The MNCV was inversely correlated with the AGE levels. We conclude that improvement of conduction slowing by AG in experimental diabetes may be through decreasing the AGE level in the peripheral tissues. Aminoguanidine may have a therapeutic potential in controlling diabetic peripheral neuropathy.
The P300 and regional cerebral blood flow were measured before and after intravenous injection of L-dopa in 10 patients with idiopathic Parkinson's disease and 10 patients with vascular parkinsonism. The P300 was measured with an evoked potential recorder using an oddball paradigm and the regional cerebral blood flow was measured using the stable xenon computed tomography method. The P300 latency was significantly longer and the regional cerebral blood flow in the cerebral cortex and basal ganglia was significantly lower in the Parkinson's disease group and the vascular parkinsonism group than in the age-matched healthy control group. The intravenous injection of L-dopa improved these abnormalities significantly in the Parkinson's disease group but did not improve these abnormalities in the vascular parkinsonism group. Cognitive function is considered to be impaired in Parkinson's disease and vascular parkinsonism and L-dopa is considered to improve it in Parkinson's disease.
We investigated the effects of neurons in the rostral and caudal ventrolateral medulla (RVL and CVL) on cerebral and renal microcirculation in rats. Rats were anesthetized with chloralose, paralyzed with tubocurarine, and artificially ventilated. Cerebral and renal blood flows (CBF and RBF) were measured simultaneously using laser-Doppler flowmetry. Chemical stimulation of the RVL neurons by microinjection of the excitatory amino acid L-glutamate increased arterial pressure (AP), whereas that of the CVL neurons decreased AP. Stimulation of the RVL neurons also elicited a stimulus-locked increase in CBF and a decrease in RBF. The percent change in CBF and RBF was dose-dependent as stimulus intensity was increased. Cerebral and renal vascular resistance (CVR and RVR) levels were calculated from changes in CBF or RBF and changes in mean AP. The percent reduction in CVR and percent elevation in RVR were also dose-dependent. Chemical stimulation of the CVL neurons elicited a stimulus-locked decrease in CBF and an increase in RBF. The percent reduction in CBF and percent elevation in CVR were dose-dependent. The percent reduction in RVR was also dose-dependent, while the percent elevation in RBF was not significant. Blood withdrawal reduced AP by a similar degree to CVL stimulation, but did not significantly decrease CBF. The results suggest that RVL and CVL neurons integrate cerebral and systemic microcirculation.